Biology subjects

Choo, Y.

Publications and source records attributed to Choo, Y..

4 recordsLinked to original sources

bioRxiv2026

A domain-general basal ganglia mechanism for inhibitory control during language comprehension

Whether controlled language processing involves domain-general or language-specific neural circuits is subject of controversial debate. We tested whether the inhibitory control of linguistic activity shares a common neural process with motor inhibition in twenty humans undergoing intra- and extracranial neural field potential recordings and deep-brain stimulation. Engaging motor and linguistic inhibition simultaneously resulted in a significant behavioral cost, suggesting a shared underlying neural process. Indeed, neural decoders trained during motor inhibition were able to decode linguistic inhibition and vice versa. Depth-electrode recordings from the subthalamic nucleus (STN), a key basal ganglia area for inhibitory control, showed increased {beta}-band (13-30 Hz) activity during both linguistic and motor inhibition. Finally, disrupting the STN via deep-brain stimulation impaired behavioral and neural signatures of both linguistic and motor inhibition. Together, these findings show that the inhibitory control of language and movement share a domain-general mechanism implemented via the subthalamic nucleus of the basal ganglia.

neuroscience↗

bioRxiv2025

Pupil dilation indexes - but does not causally influence - conscious error detection: a double-blind, placebo-controlled investigation of performance-monitoring using atomoxetine.

BackgroundConscious error detection is accompanied by error-related changes in phasic autonomic activity. This autonomic response is diminished in older age - accompanied by impairments in the conscious detection of action errors - i.e., increased error blindness. Indeed, the degree to which the autonomic response to errors declines across the lifespan is correlated with the increase in error blindness. However, the direction of causality - whether changes in autonomic reactivity are a consequence or cause of increased error blindness - is still debated. In the present study, we experimentally modulated the phasic autonomic response to action errors in healthy older adults while measuring their conscious error detection. MethodsAcross two sessions, thirty healthy older adults (60-80 years old) were given the sNRI atomoxetine or placebo in a double-blind fashion. In each session, they performed an anti-saccade task, which is commonly used to test conscious error detection. The autonomic response to errors was measured via changes in pupil dilation. A novelty-oddball task was also employed as a manipulation check. ResultsAtomoxetine reduced phasic pupil dilation to both novel stimuli in the novelty-oddball task and to action errors in the anti-saccade task. However, despite this blunting of the phasic autonomic response to errors, there were no significant differences in conscious error awareness between atomoxetine and placebo. Primary task performance was also unaffected. ConclusionsDespite its effects on phasic autonomic activity after errors, atomoxetine had no effect on conscious error detection in healthy older adults. This suggests that phasic autonomic activity is a consequence, rather than a contributing factor, to conscious error awareness. It also suggests that changes to phasic autonomic activity is unlikely to explain increased error blindness in older age.

neuroscience↗

bioRxiv2025

Exploring neural mechanisms underlying error-related impairments in active working memory suggests an adaptive shielding of contents during cognitive control

Goal-directed behavior relies on cognitive flexibility - the ability to rapidly adapt ongoing thoughts and behaviors while preserving task-relevant information. The performance monitoring system optimizes such behavior by detecting and evaluating errors, while the working memory (WM) system maintains relevant information and protects it from interference. We investigated how these two systems interact. In prior work (Wessel et al., 2022), we found that motor errors impaired active WM maintenance (Error-Related Impairment of Active working Memory; ERIAM). Here, we aimed to identify the source of ERIAM by tracking a neurophysiological marker of visual WM maintenance - the contralateral delay activity (CDA) - throughout the error-making process. Forty-two human participants maintained visual information in WM while performing a motoric task during the delay period. Consistent with prior results, a significant ERIAM effect occurred: motor errors impaired WM performance. Critically, CDA amplitudes did not differ between motor correct and error trials before the flanker task, ruling out a general performance deficit. The CDA was also unaffected immediately after flankers, ruling out a perceptual interference explanation. Significant CDA differences only emerged after motor errors, supporting a genuinely error-related origin of the ERIAM effect. Contrary to prediction, however, CDA was more disrupted after correct responses than errors, and greater disruptions predicted a smaller ERIAM effect. These findings suggest that participants might store WM in multiple states to reduce interference from errors and that the CDA dynamics reflect these adaptive shielding strategies. These findings provide new insights into the source of error-related interference in active WM.

neuroscience↗

bioRxiv2022

Right inferior frontal cortex damage impairs the initiation of inhibitory control, but not its implementation

Inhibitory control is one of the most important control functions in the human brain. Much of our understanding of its neural basis comes from seminal work showing that lesions to the right inferior frontal cortex (rIFC) increase stop-signal reaction time (SSRT), a latent variable that expresses the speed of inhibitory control. However, recent work has identified substantial limitations of the SSRT method. Notably, SSRT is confounded by trigger failures: stop-signal trials in which inhibitory control was never initiated. Such trials inflate SSRT, but are typically indicative of attentional, rather than inhibitory deficits. Here, we used hierarchical Bayesian modeling to identify stop-signal trigger failures in human rIFC lesion patients, non-rIFC lesion patients, and healthy comparisons. Furthermore, we measured scalp-EEG to detect {beta}-bursts, a neurophysiological index of inhibitory control. rIFC lesion patients showed a more than five-fold increase in trigger failure trials and did not exhibit the typical increase of stop-related frontal {beta}- bursts. However, on trials in which such {beta}-bursts did occur, rIFC patients showed the typical subsequent upregulation of {beta} over sensorimotor areas, indicating that their ability to implement inhibitory control, once triggered, is intact. These findings suggest that the role of rIFC in inhibitory control has to be fundamentally reinterpreted.

neuroscience↗